http://www.cns.nyu.edu/labs/ledouxlab/images/image_research/fear_conditioning.jpg
Adapted from (Davis, 1992)
Cohen’s d-effect sizes 95% CI and for differences in subcortical brain volumes between major depressive disorder (MDD) patients and healthy control subjects. Effect sizes were corrected for age, sex and intracranial volume (ICV). The effect size for ICV was corrected for age and sex. P<0.05 corrected. CI, confidence interval.
(a) Cohen’s d-effect sizes 95% CI for differences in subcortical brain volumes between recurrent major depressive disorder (MDD) patients and healthy control subjects (striped pattern) and between first episode MDD patients and healthy controls (no pattern). (b) Cohen’s d-effect sizes 95% CI for differences in subcortical brain volumes between early onset (⩽21) MDD patients and healthy control subjects (no pattern) and between later onset (>21) MDD patients and healthy controls (striped pattern). Effect sizes were corrected for age, sex and intracranial volume (ICV). P<0.05 corrected, P<0.05. CI, confidence interval.
“Figure 1. Neuroarchitectural Changes Induced by Repeated or Acute Stress in Rodents. (A) Repeated restraint stress (7 days) induces a reduction in the number and length of apical dendrites of pyramidal neurons (layer V) in the medial prefrontal cortex (PFC) of rats. (B) Magnified segment of dendrite from the same stressed rats, showing that repeated stress significantly decreases the number of spine synapses in medial PFC. (C) Reconstructions of representative infralimbic pyramidal neurons in mice exposed to zero (0), one (1×), or three (3×) unpredictable sessions of 10 min of forced swim stress. Apical dendritic branch length was significantly reduced after one or three stress episodes relative to controls. Adapted, with permission, from [24] (B) and [23] (C).”
Figure 3. Graphic Summary of Short- and Long-Term Functional and Neuroarchitectural Effects in Prefrontal Cortex (PFC) Synapses after Acute Footshock (FS) Stress [44]. The fast and transient increase in corticosterone (CORT) release induced by acute (40 min) FS stress was accompanied by the rapid increase in both depolarization-evoked and hypertonic sucrose-evoked (readily releasable pool) glutamate release in PFC, and the number of small excitatory synapses. The enhancement of glutamate release was sustained for up to 24 h, as well as the increased number of excitatory synapses, which normalized between 24 h and 7 days after FS. Before 24 h had elapsed from the start of FS stress, retraction of apical dendrites began and was sustained for up to 14 days. The timing of actual FS stress (40 min) is indicated by the red marker. Number of excitatory synapses and apical dendrite length are indicative and not in scale with other readouts. CORT and glutamate release data adapted from [44].
Sapolsky, Why Zebras Don’t Get Ulcers
Figure 1. Measuring reward and hedonia. Reward and pleasure are multifaceted psychological concepts. Major processes within reward (first column) consist of motivation or wanting (white), learning (blue), and – most relevant to happiness – pleasure, liking or affect (light blue). Each of these contains explicit (top rows, light yellow) and implicit (bottom rows, yellow) psychological components (second column) that constantly interact and require careful scientific experimentation to tease apart. Explicit processes are consciously experienced (e.g. explicit pleasure and happiness, desire, or expectation), whereas implicit psychological processes are potentially unconscious in the sense that they can operate at a level not always directly accessible to conscious experience (implicit incentive salience, habits and ‘liking’ reactions), and must be further translated by other mechanisms into subjective feelings. Measurements or behavioral procedures that are especially sensitive markers of each of the processes are listed (third column). Examples of some of the brain regions and neurotransmitters are listed (fourth column), as well as specific examples of measurements (fifth column), such as an example of how highest subjective life satisfaction does not lead to the highest salaries (top) [93]. Another example shows the incentive-sensitization model of addiction and how ‘wanting’ to take drugs may grow over time independently of ‘liking’ and ‘learning’ drug pleasure as an individual becomes an addict (bottom) [94].
Figure 2. Hedonic brain circuitry. The schematic figure shows the brain regions for causing and coding fundamental pleasure in rodents and humans. (a) Facial ‘liking’ and ‘disliking’ expressions elicited by sweet and bitter taste are similar in rodents and human infants. (b, d) Pleasure causation has been identified in rodents as arising from interlinked subcortical hedonic hotspots, such as in nucleus accumbens and ventral pallidum, where neural activation may increase ‘liking’ expressions to sweetness. Similar pleasure coding and incentive salience networks have also been identified in humans. (c) The so-called ‘pleasure’ electrodes in rodents and humans are unlikely to have elicited true pleasure but perhaps only incentive salience or ‘wanting’. (d) The cortical localization of pleasure coding might reach an apex in various regions of the orbitofrontal cortex, which differentiate subjective pleasantness from valence processing for aspects of the same stimulus, such as a pleasant food.
DA and GABA signaling
Expectation modulates DA signaling
DA network
Reward & Aversion Networks
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